ArticleGenetics2006
A mutation in Tac1p, a transcription factor regulating CDR1 and CDR2, is coupled with loss of heterozygosity at chromosome 5 to mediate antifungal resistance in Candida albicans.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers.
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Who cites it
218 citing papers in PubMed, 381 citations in OpenAlex.
- CRISPR-activation reveals key resistance genes and vulnerabilities of copy number variants inbioRxiv : the preprint server for biology · 2026Article
- Generation of antifungals to combat drug resistance using language models and diffusion models.Journal of advanced research · 2026Article
- Antifungal resistance: from classical mechanisms to the expanding role of acetyltransferases.Journal of biomedical science · 2026Review
- Insights on molecular drivers of phenotypic plasticity in Candidozyma auris.World journal of microbiology & biotechnology · 2026Review
- Lipid-Based Drug Delivery Systems as Emerging Tools to Overcome Antifungal Resistance.International journal of molecular sciences · 2026Review
- Estimating the distribution of fitness effects of loss of heterozygosity (LOH) events using an engineered library of Saccharomyces cerevisiae.PLoS genetics · 2026Article
- Diagnostics for human pathogenic fungal infections: Current status and future prospects.hLife · 2026Review
- Regulation of ABC Transporters and Ergosterol Biosynthesis by the Transcription Factor FvADS-1 Controls Azole Resistance and Virulence inJournal of fungi (Basel, Switzerland) · 2026Article
- Experimental Evolution of PathogenicMicroorganisms · 2026Review
- Advances in vulvovaginal candidiasis research: a comprehensive review from epidemiology, diagnosis, treatment to resistance mechanisms.Frontiers in microbiology · 2026Review
- VaginalFrontiers in microbiology · 2026Article
- Targeted loss of heterozygosity in Candida albicans using CRISPR-Cas9 reveals the functional impact of allelic variation.Genetics · 2025Article
- Fluconazole resistance andMicrobiology (Reading, England) · 2025Article
- Vaginal mycobiome characteristics and therapeutic strategies in vulvovaginal candidiasis (VVC): differentiating pathogenic species and microecological features for stratified treatment.Clinical microbiology reviews · 2025Review
- Strain background interacts with chromosome 7 aneuploidy to determine commensal and virulence phenotypes in Candida albicans.PLoS genetics · 2025Article
- Adaptive evolution ofmBio · 2025Article
- Article
- The role of gene copy number variation in antimicrobial resistance in human fungal pathogens.npj antimicrobials and resistance · 2025Review
- Transcription factor Hap2p regulates antioxidant stress responses to maintain miconazole resistance inMycology · 2025Article
- Hybrid adaptation is hampered by Haldane's sieve.Nature communications · 2024Article
158 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
TAC1, a Candida albicans transcription factor situated near the mating-type locus on chromosome 5, is necessary for the upregulation of the ABC-transporter genes CDR1 and CDR2, which mediate azole resistance. We showed previously the existence of both wild-type and hyperactive TAC1 alleles. Wild-type alleles mediate upregulation of CDR1 and CDR2 upon exposure to inducers such as fluphenazine, while hyperactive alleles result in constitutive high expression of CDR1 and CDR2. Here we recovered TAC1 alleles from two pairs of matched azole-susceptible (DSY294; FH1: heterozygous at mating-type locus) and azole-resistant isolates (DSY296; FH3: homozygous at mating-type locus). Two different TAC1 wild-type alleles were recovered from DSY294 (TAC1-3 and TAC1-4) while a single hyperactive allele (TAC1-5) was isolated from DSY296. A single amino acid (aa) difference between TAC1-4 and TAC1-5 (Asn977 to Asp or N977D) was observed in a region corresponding to the predicted activation domain of Tac1p. Two TAC1 alleles were recovered from FH1 (TAC1-6 and TAC1-7) and a single hyperactive allele (TAC1-7) was recovered from FH3. The N977D change was seen in TAC1-7 in addition to several other aa differences. The importance of N977D in conferring hyperactivity to TAC1 was confirmed by site-directed mutagenesis. Both hyperactive alleles TAC1-5 and TAC1-7 were codominant with wild-type alleles and conferred hyperactive phenotypes only when homozygous. The mechanisms by which hyperactive alleles become homozygous was addressed by comparative genome hybridization and single nucleotide polymorphism arrays and indicated that loss of TAC1 heterozygosity can occur by recombination between portions of chromosome 5 or by chromosome 5 duplication.
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